Essentially, syncope is a temporary loss of consciousness with a drop in muscle tone, resulting from a momentary reduction in blood circulation in the brain. Amongst the various types of syncope, vasovagal syncope is that which is produced by a temporary imbalance in the system for regulating vasovagal equilibrium, leading to the vagal system being activated excessively, giving rise to vasodilation and bradycardia, causing syncope.
It is generally considered that vasovagal syncope comes from a state in which the sympathetic system presents particularly high reactivity having the effect of triggering and opposing an excessive response of the parasympathetic system, leading to vasodilation, itself inducing a reduction in the filling of the ventricles and bradycardia.
The complexity of these mechanisms makes determining the etiology of vasovagal syncope awkward, and consequently makes it difficult to prescribe any appropriate pharmacological or other therapy.
Until now, only complex and invasive methods have been available for studying the behavior of the autonomic nervous system of a subject, which is thus of limited application and generally restricted to a few special cases.
Thus, Mangin et al., in “Simultaneous Analysis Of Heart Rate Variability and Myocardial Contractility During Head-up Tilt In Patients With Vasovagal Syncope,” published in the Journal of Cardiovascular Electrophysiology, Vol. 12, Issue 6, 639-644 (June 2001), have proposed using an endocardiac acceleration signal delivered by an implanted prosthesis to analyze the sympathico-vagal activity of a patient.
As described, for example, in EP-A-0 515 319 (assigned to Sorin Biomedica Cardio SpA), there exist pacemakers associated with an endocavity lead in which the distal electrode implanted at the end of the ventricle includes a micro-accelerometer suitable for measuring endocardiac acceleration. EP-A-0 655 260 (assigned to Sorin Biomedica Cardio SpA) describes one way of treating the endocavity acceleration signal delivered by that sensor situated at the end of the lead in order to detect certain cardiac disturbances and possibly trigger defibrillation therapy.
The above-identified article by Mangin et al. describes the result of clinical studies performed on a series of patients fitted with such prostheses, where attempts were made to provoke a syncope in such patients by means of a tilt-test, a test which itself is well known, having the purpose of revealing the origin of syncope that can be caused when a patient installed on a tilting table goes from a prone position to a highly inclined position, the result being considered positive if functional symptoms of syncope appear within a given length of time, including severe hypotension possibly associated with paradoxyl bradycardia.
The study reported in that article reveals a correlation between the levels of the peaks of endocardiac acceleration (PEA) and the propensity to develop syncope. Nevertheless, that study recognizes the limitation due to the small number of patients, who are necessarily patients who have received pacemakers specially provided with means for measuring endocardiac acceleration. In addition, the article draws no conclusions, whether therapeutically or diagnostically, from the correlation found between the variations in PEA and the occurrence of vasovagal syncope.